Treatments have been available since the end of 1996 which are capable of controlling multiplication of the human immunodeficiency virus (HIV), which is the cause of acquired immune deficiency syndrome (AIDS). These treatments have been generically so-called highly active anti-retroviral therapy (HAART). The current HAART characteristically consists in the combination of at least three drugs.
There are at present two families of antiretrovirals that inhibit key enzymes for viral replication and which are the reverse transcriptase inhibitors (nucleoside analogues, nucleotide analogues and nucleoside non-analogues) and the viral protease inhibitors.
However, such treatments are not capable of leading to eradication of the virus (elimination thereof) and, to keep the infection controlled they, therefore, have to be administered indefinitely, probably throughout the patient's entire lifetime.
Such treatments, of undoubted efficacy in controlling viral replication, are nevertheless not innocuous for patients, and because the exposure time thereto is, necessarily, very lengthy, their toxic effects tend to accumulate over time.
Since 1997 there began to be detected patients submitted to HAART who presented disorders not previously described in body-fat distribution, accompanied by plasma lipid level disorders.
Briefly, the patients show loss of fat in the face, buttocks, extremities and thorax, accompanied by accumulation of fat inside the abdomen, the back of the neck and in the breast area in women, together with increase plasmatic levels of cholesterol, triglycerides, lowering of HDL cholesterol (protective cholesterol) and increase of LDL cholesterol (harmful cholesterol), insulin resistance (occasionally diabetes) and occasionally arterial hypertension.
This entire set of situations is known as lipodystrophy syndrome.
Approaches to the treatment of lipodystrophy can be summed up in five broad groups:
(a) Strategies which modify the HAART components, so that this cannot be suppressed without running the risk of losing control over viral replication.
(b) Drugs (e.g. methformine, rosiglytazone) which cause sensitisation to the action of insulin.
(c) Drugs which aim to control the lipidic aspects of the syndrome, such as fibrates and statines, which can improve (though rarely normalise) plasmatic lipid disorders.
(d) Hormone treatments (e.g. growth hormones).
(e) Facial cosmetic surgery with implants to correct fat loss.
None of the treatments tested so far have shown any efficacy in reversing the disorders in body fat distribution, and the control of lipidic disorders using such measures has been incomplete.
It should be mentioned that the foregoing tested pharmacological treatments are not without toxic effects on the patient, which can, occasionally, be serious. They furthermore, mean an additional drug burden, and some of them interact in a potentially serious way with the antiretroviral drugs which HIV-infected patients cannot stop taking.
There is still, therefore, no available treatment for lipodystrophy, in particular in HIV-infected patients, which is effective and does not give rise to the disadvantages of the treatments currently known.